Articles
| Open Access |
https://doi.org/10.55640/gjmps-abcd08
AUGMENTING WITHAFERIN-A'S ANTIPROLIFERATIVE POTENTIAL AGAINST EXPERIMENTAL HEPATOCELLULAR CARCINOMA
B. Arun Babu , Assistant Project Scientist, California University, USA; 3Assistant Professor, 6Guest lecturer, University of Madras, Taramani, Chennai, T N, IndiaAbstract
Hepatocellular carcinoma (HCC) remains a significant global health concern with limited treatment options. Withaferin-A (WA), a natural compound derived from Withania somnifera, has shown promising antiproliferative effects against various cancer types, including HCC. However, its efficacy as a standalone treatment for HCC is limited. This study investigates strategies to enhance the antiproliferative activity of Withaferin-A against experimental HCC models. Using in vitro and in vivo approaches, we evaluated the synergistic effects of Withaferin-A in combination with other compounds and treatments. Results indicate that combination therapy involving Withaferin-A demonstrates enhanced antiproliferative activity against HCC cells compared to Withaferin-A alone. Furthermore, in vivo studies using experimental HCC models confirm the efficacy of combination therapy in inhibiting tumor growth and improving survival outcomes. These findings highlight the potential of combination therapy involving Withaferin-A as a promising strategy for the treatment of hepatocellular carcinoma.
Keywords
Withaferin-A, Hepatocellular carcinoma, Antiproliferative activity
References
Llovet JM, Fuster J, Bruix J. The Barcelona approach: diagnosis, staging and treatment of hepatocellular carcinoma. Liver Transpl 2004; 10:S115-120.
Fattovich G, Stroffolini T, Zagni I, Donato F. Hepatocellular carcinoma in cirrhosis: incidence and risk factors. Gastroenterology 2004; 127:S35-50.
Fisher DE. Apoptosis in cancer therapy: crossing the threshold. Cell 1994; 78:539-542.
Kaufmann SH. Induction of endonucleolytic DNA cleavage in human acute myelogenous leukemia cells by etoposide, camptothecin, and other cytotoxic anticancer drugs: a cautionary note. Cancer Res 1989; 49:5870-5878.
Lance A. Liotta. Tumor Invasion and matastases roleof the Extracellular Matrix: Rhoads Memorial Award Lecture. Can. Res 1986; 46:1-7.
Sporn MB and Harris ED. Proliferative diseases. Am J MED 1988; 70:1231- 1236.
Bravo R and Bravo HM. Existence of two populations of cycling proliferating cell nuclear antigen during the cell cycle association with DNA replication sites. J Cell Biol 1987; 105: 1549-54.
Kurki P, Ogata K, Tan EM. Monoclonal antibodies to proliferating cell nuclear antigen (PCNA) /cycling as probes for proliferating cells by immunofluorescence microscopy and flowcytometry. J Immunol Methods 1988; 109: 49-59.
Osman HG, Gabr OM, Lotfy S, Gabr S. Serum levels of Bcl-2 and cellular oxidative stress in patients with viral hepatitis. Indian J Med Microbiol 2007; 25 (4): 323-9.
Steller H. Mechanisms and genes of cellular suicide. Science 1995; 267:1445-1449.
Thompson CB. Apoptosis in the pathogenesis and treatment of disease. Science 1985; 267:
Fisher DE. Apoptosis in cancer therapy: crossing the threshold. Cell. 1994;78:539-542.
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